Pharmacology 101:
As a paramedic we are not expected to be doctors or pharmacists, however a foundational understanding of basic pharmacology is essential for recognizing what medications our patients are taking, what they are for, and what their effects are on the human body. What follows is a very brief, high-level overview of pharmacology for the prehospital provider.
Lets start with the VERY basics:
What is a drug? Technically speaking, a drug is any substance that enters the body and has an effect on metabolic processes. So... lots of things are drugs. Coffee, ASA, nicotine, THC, ETOH, and some of our favourite recreational substances are all classified as drugs; but so are other things, like sugar, or even water. All of these things affect the processes that happen in the body. In order to understand how drugs work within the human body there are 2 fundamental concepts we need to understand:
Pharmacokinetics
Pharmacodynamics
Pharmacokinetics:
Pharmacokinetics refers to the means by which a drug enters the body, moves through the body, and is excreted from the body. Drugs enter the body by inhalation, absorption, ingestion, or injection. The physical properties of plasma membranes determine how drugs are transported throughout the body.
There are four processes involved in pharmacokinetics:
Absorption: Refers to how a drug moves from the site of administration into the bloodstream.
Metabolism: This is the process of changing an absorbed drug into a form that is more likely to be excreted. This usually takes place in the liver.
Distribution: Refers to how a drug is transported through the body. Various factors play a role here including the formation of drug-protein complexes, and special barriers such as the blood-brain barrier (Adams. 2010).
Excretion: The process by which drugs are removed from the body. This may involve the renal, respiratory, or endocrine systems.
Pharmacodynamics:
Pharmacodynamics refers to how a drug changes bodily processes (Adams.2010). It focuses on the mechanism of action within the cells of the body, the resulting changes that occur, and the dose that is required. When a drug is developed, testing is done to reveal a “frequency distribution curve”. This is a graphical representation of the number of subjects who respond to a drug at various different doses. The resulting data demonstates a bell curve. This curve is used to determine the following:
The ED50: The Median Effective Dose. This is the dosage of a drug that provoked the desired response in 50% of the test subjects.
The LD50: The Median Lethal Dose. This dosage is extrapolated from test data to represent the level of a drug that would be fatal if taken by 50% of the test subjects.
The Therapeutic Index: This is the ratio of the ED50 to the LD50. If there is a large difference between the 2, a drug is said to have a wide therapeutic index.
Pharmacodynamics also focuses on 2 main attributes of drugs: Potency, and Efficacy.
Potency: A drug is said to be more potent than similar drugs if it can produce the same effects as those drugs at a lower dose.
Efficacy: Efficacy is a measurement of the magnitude of maximal response of a drug.
Pharmacodynamics is lastly concerned with drug action within the body. Drugs work by “cell-signalling” which refers to a system of communication in the body that allows cells to perceive and respond to their environment (Adams.2010). Cells receive information about their environment through membrane receptors, which are protein sites on the phospholipid bilayer that bind to external molecules. Substances that bind to these receptors are referred to as Ligands. Ligands include hormones, cytokines, neurotransmitters, and growth factors. If these substances occur naturally they are said to be endogenous. If they are introduced artificially they are exogenous. When drugs bind to these receptor sites they can have one of two effects:
Agonists: Agonists are drugs, when bound to a receptor, produce the same effect as an endogenous substance. An example would be Epinephrine, which binds to alpha and beta receptors, increasing sympathetic nervous system activity.
Antagonists: These are drugs that compete with endogenous substances in binding to receptors. They reduce the activity of an endogenous substance. A good example of this would be Naloxone, which competes for opioid receptors in the body.
Now that we have an understanding of the basic way in which drugs enter the body and are used within the cells. Lets talk about drugs for the different body systems. This is not an in depth overview, and it is expected that Paramedic students should have a solid grasp of the body systems by this point. When discussing the different classes of drugs, I will include the drug suffixes associated with them. The suffixes are a quick way to recognize what family a drug is in at a glance.
Cardiovascular Medications:
Suffix | Class | Mechanism of action |
-sartan ie: Irbesartan | Angiotensin II Receptor Blockers | Act as antagonists in the RAAS, preventing the conversion of angiotensin I into angiotensin II. This inhibits systemic vasoconstriction. It is used in the setting of Hypertension. |
-ide ie: Furosemide | Loop Diuretics | Act in the renal system, at the loop of Henle. These drugs prevent the reuptake of Na+, and therefore promote the excretion of excess fluid as urine. |
-dipine ie: Amlodipine | Calcium Channel Blockers | Inhibit the action of calcium in smooth muscle cells in the vascular system. This prevents vasoconstriction and is used to treat hypertension. CCB are also used in the treatment of contractility problems in the heart and the treatment of dysrhythmias. |
-olol ie: Bisoprolol | Beta Blocker | Antagonistically bind to Beta adrenergic receptors, reducing sympathetic response. Used to reduce heart rate and blood pressure. |
-oxin ie: Digoxin | Cardiac Glycoside | Reduce heart rate and increase force of contraction. Used in the treatment of dysrhythmias and heart failure. |
-pril ie: Ramipril | ACE inhibitor | Inhibit the conversion of angiotensinogen into angiotensin I in the RAAS. Reducing Na+ retension. Antihypertensive. |
-zosin or -losin ie: Terazosin | Alpha 1 antagonist | Inhibit the sympathetic action of alpha one adrenergic receptors. This prevents systemic vasoconstriction and reduces blood pressure. |
-statin ie: Atorvastatin | Anti-hyperlipidemic | Reduce the amount of cholesterol made by the liver, and aid in its removal from the bloodstream. |
-fil | Phosphodiesterase Inhibitor | Work by blocking the breakdown of the enzyme cGMP, which prolongs the action of nitric oxide in the bood. This leads to vasodilation. These drugs are used in the treatment of pulmonary hypertension and erectile dysfunction. |
Respiratory Medications and Steroids:
Suffix | Class | Mechanism of action |
-terol, -amol ie: Salbutamol | Beta 2 Agonist | Binds to beta 2 adrenergic receptors, triggering bronchodilation. |
-sone ie: Dexamethosone | Corticosteroid | Reduce local and systemic inflammatory responses. |
-tropium, -fenacin ie: Ipatropium | Anticholinergic | Antagonistically inhibit parasympathetic bronchoconstriction. |
-phrine ie: Epinephrine | Adrenergic Agonist | Binds to alpha and beta adrenergic receptors, triggering beta 2 induced bronchodilation and alpha 1 induced vasoconstriction which reduces angioedema. |
Antiplatelets and Anticoagulants:
Suffix | Class | Mechanism of action |
ASA (no suffix) | Platelet aggregation inhibitor (Antiplatelet) | Blocks the action of the enzyme cyclooxygenase, preventing the formation of thromboxane. This stops platelet aggregation and clot formation. |
-grel ie: Clopidogrel (Plavix) | ADP Receptor Blocker (Antiplatelet) | Works in similar fashion to ASA in inhibiting the formation of blood clots. |
-parin ie: Heparin | Anticoagulant | Works on several parts of the clotting cascade to prevent the formation of blood clots in the body. |
-arin, -adin ie: Coumadin, Warfarin | Anticoagulant | Inhibit the activity of vitamin K in the clotting cascade, preventing the formation of clots. |
-ase ie: Alteplase | Thrombolytic | Acts to convert plasminogen into plasmin, which dissolves fibrin clots throughout the body. |
Drugs for CNS disorders and Seizures:
Suffix | Class | Mechanism of action |
-pam, -lam ie: Midazolam | Benzodiazepine | Facilitate the binding of the neurotransmitter GABA to CNS receptors, triggering a parasympathetic response. Used in the treatment of seizure disorders. |
-met ie: Sinemet (Levodopa) | Dopaminergic | Restores the dompamine level in extrapyramidal areas of the brain to theraputic levels, reducing Parkinson's symptoms. Acts by preventing enzymatic breakdown of dopamine in the CNS. |
-tropine ie: Atropine | Anticholinergic | Block stimulation of cholinergic receptors by acetylcholine in the CNS. Inhibits parasympathetic response in the body. It can be used in the treatment of Parkinson's disease, bradycardias, and palliative relief of secretions. |
-pezil ie: Donepezil | Acetylcholinesterase inhibitors | Prevents the breakdown of acetylcholine in the neurons of the CNS, reducing the progression of dementias. |
-barbital ie: Phenobarbital | Barbiturate | Enhances the action of GABA in the CNS similarly to benzodiazepines, but with a very narrow therapeutic index. Is used in the treatment of some epilepsy disorders. |
-toin ie: Phenytoin | Sodium Channel Blocker | Decreases sodium influx in neurons in the CNS, reducing neurotransmission and the associated rapid depolarization seen in seizures. |
Carbamazepine | Anticonvulsant | Used in the treatment of seizure disorders. |
Lamotrigine | Anticonvulsant | Used in the treatment of seizure disorders. |
Valproic acid | Anticonvulsant | Used in the treatment of seizure disorders. |
Drugs for the treatment of psychiatric disorders:
Suffix | Class | Mechanism of action |
-pine, -mine, -line ie: Amitriptyline | Tricyclic Antidepressants | Act by blocking the reuptake of seratonin and norepinephrine in the synapse. This prolongs the activity of both neurotransmitters and is believed to help modulate mood disorders. Very narrow therapeutic index. |
-zine ie: Phenelzine | MAO inhibitors | Block the action of Monoamine Oxidase, preventing the breakdown of seratonin, norepinephrine, and dopamine. |
No real suffixes for these: Venlafaxine, Fluoxetine, Eschitalopram | SSRI/SNRI | Inhibit reuptake of seratonin and/or norepinephrine. |
Bupropion | Atypical Antidepressant | Inhibits reuptake of norepinephrine and dopamine. |
-phetamine ie: Dextroamphetamine (Dexedrine) | Amphetamine | Elicits stimulant effects in the brain via inhibition of transport proteins for seratoinin, norepinephrine, and dopamine. Prolong the action of these neurotransmitters in the synapse. |
-phenidate ie: Methylphenidate | NDRI | Inhibits reuptake of norepinephrine and dopamine at the synapse. This prolongs the effects of these neurotransmitters. |
-azine ie: Chlorpromazine | Conventional Antipsychotic (Phenothiazines) | Antagonistically blocks dopamine receptors on the synapse, reducing the positive symptoms of psychosis. |
No real suffixes for these: Haloperidol Loxapine Pimozide Thiothixene | Non-phenothiazine Antipsychotics | Work by various mechanisms to block dopamine receptors in the brain. |
No real suffixes for these: Clozapine Olanzapine Quetiapine Risperidone | Atypical Antipsychotics | All work by various mechanisms, blocking dopamine receptors. |
Drugs for the treatment of shock:
Suffix | Class | Mechanism of action |
Norepinephrine (Levophed) | Vasopressors | Binds to Alpha receptors in the CNS, causing systemic vasoconstriction. |
Analgesics and Anesthetics:
Suffix | Class | Mechanism of action |
-ine ie: Morphine, Codeine -nyl ie: Fentanyl, Carfentanyl | Opioid | Opioids bind with Mu receptors in the CNS and the PNS, blocking transmission of pain signals to the brain. |
No real suffixes: Ibuprofen Ketorolac (Toradol) ASA | NSAIDs | Inhibit the action of prostaglandins in the body, and reduce systemic inflammatory response. Have analgesic, anti-inflammatory, and antipyretic effects. |
Acetaminopen | Analgesic, Antipyretic | Inhibits the action of the enzymes COX1 and COX2, preventing prostaglandin synthesis. This reduces pain transmission to the brain and inhibits the development of fever. |
Gastrointestinal drugs:
Suffix | Class | Mechanism of action |
-idine ie: Ranitidine (Zantac) | H2 Receptor Blocker | Blocks the H2 receptors in acid producing cells in the stomach. Used to treat dyspepsia. |
-azole ie: Omeprazole | Proton pump inhibitor | Reduces the secretion of stomach acid by binding to the enzyme H+ K+ ATPase. Used to treat peptic ulcer disease and GERD. |
No real suffix: Diphenoxylate with Atropine (Lomotil) | Stool softener | Slows GI motility by reducing parasympathetic peristalsis. This allows more time for water to move into the colon and soften stools. |
-drinate ie: Dimenhydrinate | Anti-emetic | Acts on H1 receptors, inhibiting the action of histamine in the body. The specific anti-nauseant mechanism is not well understood. |
Antibiotics:
Suffix | Class | Mechanism of action |
-cillin ie: Penicillin, Amoxicillin | Penicillins (Antibiotic) | Inhibit bacterial cell wall synthesis, preventing further development of bacterial infections. |
-micin ie: Gentamicin | Tetracyclines (Antibiotic) | Inhibit bacterial protein synthesis. |
-acin ie: Ciprofloxacin | Floroquinalones (Antibiotic) | Inhibit mRNA/DNA synthesis. |
Drugs for the treatment of diabetes and other endocrine disorders:
Suffix | Class | Mechanism of action |
No real suffixes: Lantus Levemir Humalog | Exogenous Insulin | Act as direct replacement for endogenous insulin in the body, allowing circulating glucose molecules to enter the cells of the body for use. |
No real suffix: Glucagon | Exogenous Glucagon | Acts in place of endogenous glucagon, triggering the breakdown of stored glycogen in the liver into free glucose molecules. |
No real suffixes: Metformin Glyburide rosiglitazone | Oral Antihyperglycemics | Act using various mechanisms to either increase insulin release in desensitized persons, or to sensitize cell receptors to insulin. Used in the treatment of NIDDM. |
-thyroxine ie: Levothyroxine | Replacement hormone | Replacement of thyroid hormone in the setting of hypothyroidism. |
This is neither an exhaustive list, nor does it begin to explain the complex processes of how each drug works. However, it is a basic starting point to understanding how drug classes relate to one another and how to recognize what type of drug you are dealing with when you read a patient's medication list.
To make things a bit easier, here is a list of the most common medications you are likely to encounter:
Cardiovascular |
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Respiratory |
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“Blood thinners” |
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CNS and Seizures |
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Psychiatric |
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Antibiotics |
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Endocrine |
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Sources used:
Adams, Michael et al. Pharmacology for Nurses. 2010. Pearson. Toronto.
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